Reconciling Conflicting Approaches for the Tunneling Time Delay in Strong Field Ionization.

Several recent attoclock experiments have investigated the fundamental question of a quantum mechanically induced time delay in tunneling ionization via extremely precise photoelectron momentum spectroscopy. The interpretations of those attoclock experimental results were controversially discussed, because the entanglement of the laser and Coulomb field did not allow for theoretical treatments without undisputed approximations. The method of semiclassical propagation matched with the tunneled wave function, the quasistatic Wigner theory, the analytical R-matrix theory, the backpropagation method, and the under-the-barrier recollision theory are the leading conceptual approaches put forward to treat this problem, however, with seemingly conflicting conclusions on the existence of a tunneling time delay. To resolve the contradicting conclusions of the different approaches, we consider a very simple tunneling scenario which is not plagued with complications stemming from the Coulomb potential of the atomic core, avoids consequent controversial approximations and, therefore, allows us to unequivocally identify the origin of the tunneling time delay.

Limits of Strong Field Rescattering in the Relativistic Regime.

Recollision for a laser driven atomic system is investigated in the relativistic regime via a strong field quantum description and Monte Carlo semiclassical approach. We find the relativistic recollision energy cutoff is independent of the ponderomotive potential U_{p}, in contrast to the well-known 3.2U_{p} scaling. The relativistic recollision energy cutoff is determined by the ionization potential of the atomic system and achievable with non-negligible recollision flux before entering a "rescattering free" interaction. The ultimate energy cutoff is limited by the available intensities of short wavelength lasers and cannot exceed a few thousand Hartree, setting a boundary for recollision based attosecond physics.

Nature of early appearing, carcinogen-induced liver lesions to iron accumulation.

A technique for induction of iron accumulation in hepatocytes of rats was used to identify early carcinogen-induced lesions by their histochemical absence of iron. Foci of iron-free altered hepatocytes produced by the feeding of N-2-fluorenylacetamide (FAA) for 3 weeks were composed of cells that were replicating when surrounding iron-containing hepatocytes were not, and that responded to a mitotic stimulus when surrounding hepatocytes were inhibited or showed a delayed response. Thus these lesions represented focal hyperplastic overgrowths. The iron-free hyperplastic foci developed into hyperplastic areas that progressed with longer feeding of FAA to form hyperplastic nodules. The lack of iron was a sensitive and reliable marker for hyperplastic lesions, which also permitted their identification in the fresh state. Both early hyperplastic lesions and nodules were often resistant to the necrogenic effects of dimethylnitrosamine, as well as to the antireplicative effect of FAA. The selection of such cells resistant to the toxic effects of carcinogens may be important in the pathogenesis of liver neoplasia.

Differences in growth of transplants of liver, liver hyperplastic nodules, and hepatocellular carcinomas in the mammary fat pad.

Transplantation of fragments of normal rat liver autologously and isologously into the inguinal mammary fat pad permitted survival for up to 75% of grafts for 38 weeks, the longest interval studied. Similarly transplanted hepatocarcinomas grew rapidly and progressively in this site. Neither autologous or isologous transplants of liver hyperplastic nodules displayed obvious growth, although like normal liver, they also persisted for up to 38 weeks. Some persisting hyperplastic cells retained certain characteristic features, but others appeared to revert to a normal morphology. Thus, there is a stage in which hyperplastic cells do not possess the progressive growth ability of neoplastic cells and appear to be capable of reversion to a normal phenotype.